Autophagy and Hallmarks of Cancer

Autophagy is a catabolic program that is responsible for the degradation of dysfunctional or unnecessary proteins and organelles to maintain cellular homeostasis. Mechanistically, it involves the formation of double-membrane autophagosomes that sequester cytoplasmic material and deliver it to lysoso...

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Published inCritical reviews in oncogenesis Vol. 23; no. 5-6; p. 247
Main Authors Huang, Tianzhi, Song, Xiao, Yang, Yongyong, Wan, Xuechao, Alvarez, Angel A, Sastry, Namratha, Feng, Haizhong, Hu, Bo, Cheng, Shi-Yuan
Format Journal Article
LanguageEnglish
Published United States 2018
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Abstract Autophagy is a catabolic program that is responsible for the degradation of dysfunctional or unnecessary proteins and organelles to maintain cellular homeostasis. Mechanistically, it involves the formation of double-membrane autophagosomes that sequester cytoplasmic material and deliver it to lysosomes for degradation. Eventually, the material is recycled back to the cytoplasm. Abnormalities of autophagy often lead to human diseases, such as neurodegeneration and cancer. In the case of cancer, increasing evidence has revealed the paradoxical roles of autophagy in both tumor inhibition and tumor promotion. Here, we summarize the context-dependent role of autophagy and its complicated molecular mechanisms in the hallmarks of cancer. Moreover, we discuss how therapeutics targeting autophagy can counter malignant transformation and tumor progression. Overall, the findings of studies discussed here shed new light on exploiting the complicated mechanisms of the autophagic machinery and relevant small-molecule modulators as potential antitumor agents to improve therapeutic outcomes.
AbstractList Autophagy is a catabolic program that is responsible for the degradation of dysfunctional or unnecessary proteins and organelles to maintain cellular homeostasis. Mechanistically, it involves the formation of double-membrane autophagosomes that sequester cytoplasmic material and deliver it to lysosomes for degradation. Eventually, the material is recycled back to the cytoplasm. Abnormalities of autophagy often lead to human diseases, such as neurodegeneration and cancer. In the case of cancer, increasing evidence has revealed the paradoxical roles of autophagy in both tumor inhibition and tumor promotion. Here, we summarize the context-dependent role of autophagy and its complicated molecular mechanisms in the hallmarks of cancer. Moreover, we discuss how therapeutics targeting autophagy can counter malignant transformation and tumor progression. Overall, the findings of studies discussed here shed new light on exploiting the complicated mechanisms of the autophagic machinery and relevant small-molecule modulators as potential antitumor agents to improve therapeutic outcomes.
Author Sastry, Namratha
Alvarez, Angel A
Wan, Xuechao
Feng, Haizhong
Cheng, Shi-Yuan
Huang, Tianzhi
Song, Xiao
Hu, Bo
Yang, Yongyong
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  surname: Huang
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  givenname: Xiao
  surname: Song
  fullname: Song, Xiao
  organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL
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  givenname: Yongyong
  surname: Yang
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  givenname: Xuechao
  surname: Wan
  fullname: Wan, Xuechao
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  surname: Alvarez
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  surname: Sastry
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  givenname: Haizhong
  surname: Feng
  fullname: Feng, Haizhong
  organization: State Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
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  givenname: Bo
  surname: Hu
  fullname: Hu, Bo
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  givenname: Shi-Yuan
  surname: Cheng
  fullname: Cheng, Shi-Yuan
  organization: Ken & Ruth Davee Department of Neurology, Lou & Jean Malnati Brain Tumor Institute, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL
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Snippet Autophagy is a catabolic program that is responsible for the degradation of dysfunctional or unnecessary proteins and organelles to maintain cellular...
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StartPage 247
SubjectTerms Animals
Autophagosomes
Autophagy - drug effects
Autophagy - genetics
Biomarkers
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Drug Resistance, Neoplasm
Energy Metabolism
Epigenesis, Genetic
Humans
Molecular Targeted Therapy
Neoplasm Invasiveness
Neoplasm Metastasis
Neoplasms - diagnosis
Neoplasms - etiology
Neoplasms - metabolism
Neoplasms - therapy
RNA Processing, Post-Transcriptional
Transcription, Genetic
Title Autophagy and Hallmarks of Cancer
URI https://www.ncbi.nlm.nih.gov/pubmed/30311559
Volume 23
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